Diuretics Flashcards
What is the class for Acetazolamide (Diamox)
Carbonic anhydrase inhibitors
What is the mechanism for Acetazolamide (Diamox)
Inhibits luminal carbonic anhydrase at proximal tubule –> less activity of Na/H antiporter, decreased HCO3 and Na+ (and water) reabsorption
What are the therapeutics for Acetazolamide (Diamox)
Decrease intraocular volume/pressure and the prevention and treatment of mountain sickness
What are the important side effects for Acetazolamide (Diamox)
Increased K+ excretion and metabolic acidosis
What are the other side effects for Acetazolamide (Diamox)
Hepatic encephalopathy, BM depression, skin toxicity, allergic reactions
What are the miscellaneous for Acetazolamide (Diamox)
Contraindicated in cirrhotic patients; FeNa = 5%
What is the class for Methazolamide (Neptazane)
Carbonic anhydrase inhibitors
What is the mechanism for Methazolamide (Neptazane)
Inhibits luminal carbonic anhydrase at proximal tubule –> less activity of Na/H antiporter, decreased HCO3 and Na+ (and water) reabsorption
What are the therapeutics for Methazolamide (Neptazane)
Decrease intraocular volume/pressure and the prevention and treatment of mountain sickness
What are the important side effects for Methazolamide (Neptazane)
Increased K+ excretion and metabolic acidosis
What are the other side effects for Methazolamide (Neptazane)
Hepatic encephalopathy, BM depression, skin toxicity, allergic reactions
What are the miscellaneous for Methazolamide (Neptazane)
Contraindicated in cirrhotic patients; FeNa = 5%
What is the class for Dichlorphenamide (Daranide)
Carbonic anhydrase inhibitors
What is the mechanism for Dichlorphenamide (Daranide)
Inhibits luminal carbonic anhydrase at proximal tubule –> less activity of Na/H antiporter, decreased HCO3 and Na+ (and water) reabsorption
What are the therapeutics for Dichlorphenamide (Daranide)
Decrease intraocular volume/pressure and the prevention and treatment of mountain sickness
What are the important side effects for Dichlorphenamide (Daranide)
Increased K+ excretion and metabolic acidosis
What are the other side effects for Dichlorphenamide (Daranide)
Hepatic encephalopathy, BM depression, skin toxicity, allergic reactions
What are the miscellaneous for Dichlorphenamide (Daranide)
Contraindicated in cirrhotic patients; FeNa = 5%
What is the class for Aminophylline
Bronchodilator (Methylxanthine)
What is the mechanism for Aminophylline
Phosphodiesterase inhibition and enhanced signalling via increased cAMP and cGMP; works at proximal tubule; decreased HCO3 and Na+ (and water) reabsorption
What are the therapeutics for Aminophylline
Reduce inflammation and bronchospasm in moderate to severe asthma, night symptoms; NOT as diuretic
What are the important side effects for Aminophylline
Larger doses give nausea, vomiting, CNS stimulation or seizures, tachycardia/arrythmias
What are the miscellaneous for Aminophylline
FeNa = 5%; aminophylline = theophylline + ethyelenediamine (solubility agent); metabolized by liver; cimetidine and quinoline increase blood levels
What is the class for Mannitol (Osmitrol)
Osmotic diuretic
What is the mechanism for Mannitol (Osmitrol)
Opposes water and sodium reabsorption at proximal tubule –> increased osmolarity of tubular fluid
What are the therapeutics for Mannitol (Osmitrol)
Increased clearance of drugs, minimize renal failure (shock or surgery), decrease intraocular or intracranial pressures, diagnose oliguria
What are the important side effects for Mannitol (Osmitrol)
Risk of pulmonary edema
What are the miscellaneous for Mannitol (Osmitrol)
FeNa = 5%; must give IV; other osmotic diuretics include glucose, urea, isorbide
What is the class for Furosemide (Lasix)
Loop diuretic (- charge)
What is the mechanism for Furosemide (Lasix)
Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption, resultant K+ loss
What are the therapeutics for Furosemide (Lasix)
Crisis edema (pulmonary, CHF, cirrhosis), hypercalcemia, drug toxicity/OD; severe hypertension in setting of CHF or cirrhosis
What are the important side effects for Furosemide (Lasix)
Hypokalemia/hypocalcemia/hypomagnesemia (–> arrhythmia), contraction alkalosis, increased BUN & creatinine, ototoxicity (esp. w/aminoglycoside)
What are the other side effects for Furosemide (Lasix)
Hyper -glycemia, -lipidemia, -uricemia; hypo -magnesia, -natremia; gout, photosensitivity, nephrocalcinosis, drug interactions; erectile dysfunction
What are the miscellaneous for Furosemide (Lasix)
FeNa = 25%; eventually causes increase in PT reabsorption,decreases positive & negative free water clearance; decreases cortex-medulla molarity gradient; avoid NSAIDs, take before salty meals, reduce salt intake; useful in patients with renal insufficiency (GFR < 30-40)
What is the class for Bumetanide (Bumex)
Loop diuretic (- charge)
What is the mechanism for Bumetanide (Bumex)
Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption, resultant K+ loss
What are the therapeutics for Bumetanide (Bumex)
Crisis edema (pulmonary, CHF, cirrhosis), hypercalcemia, drug toxicity/OD; severe hypertension in setting of CHF or cirrhosis
What are the important side effects for Bumetanide (Bumex)
Hypokalemia/hypocalcemia/hypomagnesemia (–> arrhythmia), contraction alkalosis, increased BUN & creatinine, ototoxicity (esp. w/aminoglycoside)
What are the other side effects for Bumetanide (Bumex)
Hyper -glycemia, -lipidemia, -uricemia; hypo -magnesia, -natremia; gout, photosensitivity, nephrocalcinosis, drug interactions; erectile dysfunction
What are the miscellaneous for Bumetanide (Bumex)
FeNa = 25%; eventually causes increase in PT reabsorption,decreases positive & negative free water clearance; decreases cortex-medulla molarity gradient; avoid NSAIDs, take before salty meals, reduce salt intake; useful in patients with renal insufficiency (GFR < 30-40)
What is the class for Torsemide (Demadex)
Loop diuretic (- charge)
What is the mechanism for Torsemide (Demadex)
Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption, resultant K+ loss
What are the therapeutics for Torsemide (Demadex)
Crisis edema (pulmonary, CHF, cirrhosis), hypercalcemia, drug toxicity/OD; severe hypertension in setting of CHF or cirrhosis
What are the important side effects for Torsemide (Demadex)
Hypokalemia/hypocalcemia/hypomagnesemia (–> arrhythmia), contraction alkalosis, increased BUN & creatinine, ototoxicity (esp. w/aminoglycoside)
What are the other side effects for Torsemide (Demadex)
Hyper -glycemia, -lipidemia, -uricemia; hypo -magnesia, -natremia; gout, photosensitivity, nephrocalcinosis, drug interactions; erectile dysfunction
What are the miscellaneous for Torsemide (Demadex)
FeNa = 25%; eventually causes increase in PT reabsorption,decreases positive & negative free water clearance; decreases cortex-medulla molarity gradient; avoid NSAIDs, take before salty meals, reduce salt intake; useful in patients with renal insufficiency (GFR < 30-40)
What is the class for Ethacrynic acid (Edecrin)
Loop diuretic (- charge)
What is the mechanism for Ethacrynic acid (Edecrin)
Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption, resultant K+ loss
What are the therapeutics for Ethacrynic acid (Edecrin)
Crisis edema (pulmonary, CHF, cirrhosis), hypercalcemia, drug toxicity/OD; severe hypertension in setting of CHF or cirrhosis; sulfa-free
What are the important side effects for Ethacrynic acid (Edecrin)
Hypokalemia/hypocalcemia/hypomagnesemia (–> arrhythmia), contraction alkalosis, increased BUN & creatinine, ototoxicity (esp. w/aminoglycoside)
What are the other side effects for Ethacrynic acid (Edecrin)
Hyper -glycemia, -lipidemia, -uricemia; hypo -magnesia, -natremia; gout, photosensitivity, nephrocalcinosis, drug interactions; erectile dysfunction
What are the miscellaneous for Ethacrynic acid (Edecrin)
FeNa = 25%; eventually causes increase in PT reabsorption,decreases positive & negative free water clearance; decreases cortex-medulla molarity gradient; avoid NSAIDs, take before salty meals, reduce salt intake; useful in patients with renal insufficiency (GFR < 30-40)
What is the class for Chlorothiazide (Chlotride)
Thiazide diuretic (- charge)
What is the mechanism for Chlorothiazide (Chlotride)
Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
What are the therapeutics for Chlorothiazide (Chlotride)
HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus
What are the important side effects for Chlorothiazide (Chlotride)
Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine
What are the other side effects for Chlorothiazide (Chlotride)
Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions
What are the miscellaneous for Chlorothiazide (Chlotride)
FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance
What is the class for Hydrochlorothiazide (Microzide)
Thiazide diuretic (- charge)
What is the mechanism for Hydrochlorothiazide (Microzide)
Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
What are the therapeutics for Hydrochlorothiazide (Microzide)
HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus
What are the important side effects for Hydrochlorothiazide (Microzide)
Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine
What are the other side effects for Hydrochlorothiazide (Microzide)
Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions
What are the miscellaneous for Hydrochlorothiazide (Microzide)
FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance
What is the class for Chlorthalidone (Thalitone)
Thiazide-like diuretic
What is the mechanism for Chlorthalidone (Thalitone)
Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
What are the therapeutics for Chlorthalidone (Thalitone)
Reduce stroke risk, CHF events; HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus
What are the important side effects for Chlorthalidone (Thalitone)
Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine
What are the other side effects for Chlorthalidone (Thalitone)
Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions
What are the miscellaneous for Chlorthalidone (Thalitone)
FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance
What is the class for Quinethazone (Hydromox)
Thiazide-like diuretic
What is the mechanism for Quinethazone (Hydromox)
Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
What are the therapeutics for Quinethazone (Hydromox)
HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus
What are the important side effects for Quinethazone (Hydromox)
Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine
What are the other side effects for Quinethazone (Hydromox)
Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions
What are the miscellaneous for Quinethazone (Hydromox)
FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance
What is the class for Metolazone (Zaroxolyn)
Thiazide-like diuretic
What is the mechanism for Metolazone (Zaroxolyn)
Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
What are the therapeutics for Metolazone (Zaroxolyn)
HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus
What are the important side effects for Metolazone (Zaroxolyn)
Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine
What are the other side effects for Metolazone (Zaroxolyn)
Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions
What are the miscellaneous for Metolazone (Zaroxolyn)
FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance
What is the class for Indapamide (Lozol)
Thiazide-like diuretic
What is the mechanism for Indapamide (Lozol)
Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
What are the therapeutics for Indapamide (Lozol)
HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus
What are the important side effects for Indapamide (Lozol)
Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine
What are the other side effects for Indapamide (Lozol)
Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions
What are the miscellaneous for Indapamide (Lozol)
FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance
What is the class for Amiloride (Midamor)
K+-sparing diuretic; renal ENaC inhibitor (+ charge)
What is the mechanism for Amiloride (Midamor)
Blocks Na channel and Na/H antiporter in lumenal membrane at the late distal tubule and collecting duct –> decreased K+ secretion and distal tubule acid secretion, increased Ca++ absorption
What are the therapeutics for Amiloride (Midamor)
Combination with other diuretics to prevent hypokalemia; edema, idiopathic hypercalciuria (stones); lithium-induced polyuria & toxicity, Liddle syndrome, mucocilliary clearance
What are the important side effects for Amiloride (Midamor)
Hyperkalemia in patients with renal failure or on ACE inhibitors
What are the miscellaneous for Amiloride (Midamor)
Contraindicated in patients with renal failure (hyperkalemia), ACEi/ARB use; FeNa = 2%
What is the class for Triamterene (Dyrenium)
K+-sparing diuretic; renal ENaC inhibitor (+ charge)
What is the mechanism for Triamterene (Dyrenium)
Blocks Na channel and Na/H antiporter in lumenal membrane at the late distal tubule and collecting duct –> decreased K+ secretion and distal tubule acid secretion, increased Ca++ absorption
What are the therapeutics for Triamterene (Dyrenium)
Combination with other diuretics to prevent hypokalemia; edema
What are the important side effects for Triamterene (Dyrenium)
Hyperkalemia in patients with renal failure or on ACE inhibitors
What are the other side effects for Triamterene (Dyrenium)
Megaloblastic anemia in patients with liver cirrhosis
What are the miscellaneous for Triamterene (Dyrenium)
Contraindicated in patients with renal failure (hyperkalemia); FeNa = 2%
What is the class for Spironolactone (Aldactone)
K+-sparing diuretic; aldosterone receptor antagonist
What is the mechanism for Spironolactone (Aldactone)
Competes for aldosterone receptor, inhibiting mRNA transcription and translation –> decreased Na and K channels, decreased number and activity of Na-K-ATPase pumps in the late distal tubule and collecting duct –> decreased K+ secretion, distal tubule acid secretion
What are the therapeutics for Spironolactone (Aldactone)
Reduction in CHF mortality (30% in NYHA class III and IV); combination with other diuretics to prevent hypokalemia; edema; primary and secondary aldosteronism; hypertension; anti-testosterone agent
What are the important side effects for Spironolactone (Aldactone)
Hyperkalemia in patients with renal failure or on ACE inhibitors; male patients may have gynecomastia, erectile dysfunction, and loss of libido; female patients may have amenorrhea, breast soreness, and oligomenorrhea
What are the miscellaneous for Spironolactone (Aldactone)
Contraindicated in patients with renal failure (hyperkalemia); FeNa = 2%; requires a salt-restricted diet; only drug not requiring tubular lumen access
What is the class for Conivaptan (Vaprisol)
Aquaretic
What is the mechanism for Conivaptan (Vaprisol)
Vasopressin (ADH) receptor antagonist working at collecting duct –> increased free water excretion
What are the therapeutics for Conivaptan (Vaprisol)
Hyponatremia (SIADH, CHF)
What are the miscellaneous for Conivaptan (Vaprisol)
New drug class with unproven clinical benefit
What is the class for Tolvaptan (Samsca)
Aquaretic
What is the mechanism for Tolvaptan (Samsca)
Vasopressin (ADH) receptor antagonist working at collecting duct –> increased free water excretion
What are the therapeutics for Tolvaptan (Samsca)
Hyponatremia (SIADH, CHF)
What are the miscellaneous for Tolvaptan (Samsca)
New drug class with unproven clinical benefit